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嗜酸氧化亚铁硫杆菌的分歧染色体砷操纵子受一种非典型的砷阻遏蛋白调控。

The divergent chromosomal ars operon of Acidithiobacillus ferrooxidans is regulated by an atypical ArsR protein.

作者信息

Butcher Bronwyn G, Rawlings Douglas E

机构信息

Department of Microbiology, University of Stellenbosch, Private Bag X1, Matieland 7602, South Africa1.

出版信息

Microbiology (Reading). 2002 Dec;148(Pt 12):3983-3992. doi: 10.1099/00221287-148-12-3983.

DOI:10.1099/00221287-148-12-3983
PMID:12480902
Abstract

The chromosomal arsenic-resistance (ars) operon of Acidithiobacillus ferrooxidans is atypical in that it is divergent, with its arsCR and arsBH genes transcribed in opposite directions. Furthermore, the amino-acid sequence of the putative ArsR-like regulator of the ars operon is not conserved in regions that have been shown to be responsible for binding to arsenic. Instead, the ArsR-like protein of At. ferrooxidans is related to a group of unstudied ArsR-like proteins that have been found to be associated with chromosomal ars-like operons identified during genome-sequencing projects. Using arsB-lacZ, arsR-lacZ and arsC-lacZ fusions, it was shown that the ArsR-like protein of At. ferrooxidans is a repressor of the arsBH and arsRC genes of this organism, and that induction of gene expression took place when either AsIII (arsenite) or AsV (arsenate) were added. Deletion of 19 aa from the C terminus of the 118 aa ArsR protein did not affect the regulation of its activity, but deletion of an additional 28 aa inactivated ArsR. Northern-blot hybridization suggested that on induction of expression, the arsRC genes were transcribed in greater quantities than the arsBH genes, but that the level of induction was not affected by the form of arsenic added (AsIII or AsV).

摘要

嗜酸氧化亚铁硫杆菌的染色体抗砷(ars)操纵子是非典型的,因为它是发散型的,其arsCR和arsBH基因以相反方向转录。此外,ars操纵子假定的类ArsR调节因子的氨基酸序列在已被证明负责与砷结合的区域并不保守。相反,嗜酸氧化亚铁硫杆菌的类ArsR蛋白与一组未被研究的类ArsR蛋白相关,这些蛋白已被发现与基因组测序项目中鉴定出的染色体ars样操纵子有关。使用arsB-lacZ、arsR-lacZ和arsC-lacZ融合体,结果表明嗜酸氧化亚铁硫杆菌的类ArsR蛋白是该生物体arsBH和arsRC基因的阻遏物,并且当添加AsIII(亚砷酸盐)或AsV(砷酸盐)时会发生基因表达的诱导。从118个氨基酸的ArsR蛋白的C末端缺失19个氨基酸并不影响其活性的调节,但再缺失28个氨基酸会使ArsR失活。Northern印迹杂交表明,在诱导表达时,arsRC基因的转录量比arsBH基因多,但诱导水平不受添加的砷的形式(AsIII或AsV)的影响。

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